High-Density Lipoprotein Cholesterol Concentrations and Postheparin Hepatic and Lipoprotein Lipases in Obesity: Relationships with Plasma Insulin Levels
The concentration of high-density lipoprotein (HDL) cholesterol in patients with severe obesity is generally subnormal. The exact mechanism linking obesity with reduced levels of HDL cholesterol remains unclear. In this study we evaluated the postheparin plasma lipolytic enzymes lipoprotein lipase (LPL) and hepatic lipase (HL) in a group of 24 obese women compared with controls and analyzed the interrelationships between insulin, postheparin lipolytic enzymes and HDL subfractions. Total HDL cholesterol was significantly lower in the obese subjects than in the controls, and the difference was mainly due to HDL2 cholesterol concentrations. Mean fasting glucose, insulin and the summated means of glucose (Σ glucose) after the oral glucose tolerance test (OGTT) were not significantly different in the two groups. The summated means of insulin (Σ IRI) after the OGTT were significantly higher in the obese women than in the controls. LPL, HL and the HL-to-LPL ratio were significantly higher in the obese women than in the controls. HL and LPL correlated positively with Σ glucose, Σ IRI and body mass index (BMI) and negatively with plasma triglycerides. Partial correlation analysis demonstrated that, when exposed to similar Σ IRI values, HL and LPL were no longer correlated with Σ glucose, plasma triglycerides and BMI. HDL2 cholesterol levels were negatively correlated with HL, posthepatic plasma lipolytic activity, Σ glucose, plasma triglycerides and BMI. HDL2 cholesterol concentrations were directly correlated with LPL. Partial correlation analysis showed that when exposed to similar HL and LPL values, HDL2 cholesterol values were no longer correlated with Σ glucose, Σ IRI, plasma triglycerides and BMI. Therefore, our results demonstrate that the low HDL2 cholesterol levels found in obese women may be related to the high levels of HL and to the high HL-to-LPL ratio which in turn could be determined by the peripheral insulin resistance.